The proposed research will examine the neurobiological bases of impaired facial movement and emotional expressiveness in autism. Individuals with autism typically have significant impairments in emotional expression, including limited range and inappropriate use of facial expressions to communicate affect and intentions. Research on facial imitation and neurological functioning in autism suggests that impairment in affective facial expression may be due in part to an underlying motor dysfunction. The proposed research will test two competing models of impaired facial motility in autism: dysfunction of brainstem structures that control the musculature of facial expression versus neurological dysfunction at a cortical level. These aims will be examined in two samples: children with high functioning autism compared to typically developing children matched on age, VIQ, gender, and race, and children with low functioning autism similarly matched to children with non-specific mental retardation. Facial motility will be examined through a quantitative analysis of discrete facial movements and the coordination of these movements in affective facial expressions. Nonmeaningful facial expressions will be assessed during imitation of movements that correspond to specific branches of the facial nerve. Affective facial expressions will be measured during spontaneous, elicited, and imitated expressions of six canonical emotions. The communicative value of emotional expressions will also be assessed through qualitative analyses of participants' expressions by na'fve raters. Models of neurological involvement in facial expressiveness will further be examined through a comprehensive and quantitative evaluation of cranial nerve function. Finally, this project will examine several early developmental genes that are important in the formation and function of the brainstem and cerebellum, and thus may influence facial movement abnormalities in autism. By specifying the nature of impaired facial motility in autism, this research will have implications for early intervention and may help in the identification of endophenotypes of this disorder.